Rationalizing your Biology

I have said it many times; most of our lives is a rationale for our biology.  Years ago I thought that meant genetic tendencies.  Now I know better.  Most of our lives is a giant rationale for our epigenetics.  And that is set early on. Why not genetics?  Because early experience messes with the gene and alters its genetic destination.  And in my experience, which is now 60 years of therapy, it is epigenetics that really counts, building on the crucible of the genes.

The genes do respond but they are usurped by experience and their evolution is diverted.  It is the detour that remains and controls.  It looks like genetics and in some sense it is; on the other hand, it is not.  And what kills so many of us is EPIGENETICS.  You fate is sealed in the womb and at birth.  That seems exaggerated, hyperbole, but I think it is true, which is why we have to reorient everyone to much better gestation and birth practices.


For example, there is more and more evidence that some cancers and Alzheimers derive from womb-life and infancy.  And if those early experiences are so strong, they most certainly drive behavior; hence, neurosis.  So what are these experiences?  I have written long and hard about them, but let’s take one two.  Being stuck in the womb:  first, a  mother drinks and takes drugs and/or is excessively hyper.  The fetus cannot escape this. He is stuck, undefended and unable to run away and escape.  You may think this is rare but a speedy carrying mother is not rare. There are studies that show that speedy mom translates to speedy child.  Just as a depressed mom leads to a “downer” child.  These experiences eventually take precedence over pure genetics and  determine our lives.    Now, we compound this with a birth where the baby is drugged or blocked cannot get out and into life on this planet. He is stuck and blocked again: compounded.  So what does he do later on in stalled traffic or long lines for a theater.  He has to move, to steal a place or find a way around.  He is driven by experience, very early experience that is ineluctable.  And later, he gets married and his wife won’t do he wants immediately.  He goes into a rage.  He “cannot through” to her.  She is blocking his way.    You get it,  “epigenetics. “

These are not genetic tendencies but they do play on the genes already in place.

Another example:  A mother takes tranquilizers because her doctor says it cannot hurt her baby.  So he learns a depressive/suppressive lifestyle.  And when he tries to get born the mother is heavily anesthetized because she wants no pain at all.  But, alas, the baby is also anesthetized.  His being constantly drugged during gestation with the mother’s tranquilizers already sets up a biologic tendency.  Then he cannot help himself to get born because he is so drugged.  The whole biologic balance shifts so that he is moved to dominance of the parasympathetic nervous system.    He is a “drag” in every way.  He is not a self-starter because he could not be.  He gives up easily because he had to in order to save his life.  Too much exertion when there was so little available oxygen made things dangerous.  His blood circulation was compromised.  The blood vessels severely contracted to conserve oxygen and now we have the beginning of a life-long migraine.  Or high blood pressure, as everything had to be internalize and repressed.  And so he doesn’t like exercise, doesn’t like to go and do. Has little energy so that every little task is overwhelming.

Now this does like genetics but only if we discount experience.  And if you leave out epigenetics you have no other choice but to choose genetics.  Guess what happens in psychotherapy; yep, no focus on epigenetics because no awareness of the role of very early life experience.  So what happened when you were six? Is about as far as they go, and they leave out, what?  Epigenetics.

Epigenetics and Primal Therapy: The Cure for Neurosis (Part 1/20)

This is the first part of a series I wrote on Epigenetics and Primal Therapy. The whole article will publish soon in the "Activitas Nervosa Superior" Journal of the World Psychiatry Association (http://www.activitas.org/)



Sometimes I realize I am getting science-heavy but what is happening today is so exciting, especially since it supports what I have been writing about for almost 50 years. Almost every week, it seems, scientists announce new research confirming much of the primal position. This is especially true in the burgeoning field of epigenetics, the study of how experience changes an individual’s genetic code, previously considered inalterable. An article recapping the groundbreaking work by pioneering researchers from McGill University in Montreal proclaimed that “the emerging field of epigenetics is revolutionizing the study of mental health – and challenging the belief that DNA is destiny”(1). 

 Moreover, in terms of the history of science, the new developments augur the convergence of previously distinct fields, psychology and biology. In one report regarding research that shows a link between early-life adversity and changes in a person’s genetic make-up, the Canadian researchers come to this sweeping conclusion: “Epigenetics could serve as a bridge between the social sciences and the biological sciences, allowing a truly integrated understanding of human health and behavior.” (McGowan & Szyf, 2010, p. 71) In short, there is a growing understanding that mental illness has a crucial physical component, which has been a basic tenet of Primal Theory from the start. We have always maintained that neurosis is a disturbance of mind and body. And in our treatment, both mind and body must be involved for a cure. Now, science is showing us how that is possible at a cellular level. Unlike genetic mutations, the researchers state, “epigenetic alterations are potentially reversible” (McGowan & Szyf, 2010, p. 66). And that is the most promising finding of all. 

 I have discussed epigenetics in my blog and my books, about how adversity early on changes the switches for key genes that then serves to compound repression or inhibition. These switches turn the gene on or off, and thus help set in what seem like genetic changes. In Primal terms, it is the mechanism of closing the gates of feeling or opening them. And there are different chemicals that accompany the epigenetic events, methyl and acetyl groups, for example. The critical work in this field shows how imprints can be passed down through generations – from parent to child and grandchild – primarily through the biochemical processes known as methylation and acetylation. We need to differentiate, however, between healthy and unhealthy methylation. Under normal conditions, methylation is a necessary and naturally occurring process that helps regulate the expression of an individual’s genetic make-up. But excess methylation becomes pathological and leads to disease. The process goes awry when the individual suffers physical or psychological trauma, especially in the womb and in infancy. It seems that for each and every pain we endure during gestation and at birth there is a change in the chemicals that enhance the repression of pain. When the pain or adversity is prolonged, the system is overtaxed and we now have the mechanism of leaky gates; that is, repression begins to falter due to an overload of chronic pain. 

 It is the consistency of the pain that causes the overload. There is a limit that the brain can handle. Beyond that, the gates become vulnerable and do not do well. It takes very little trauma after that to produce a symptom such as ADD, Attention Deficit Disorder. The chemical methyl group is recruited when there is a traumatic event, and helps embed that memory. It seems that when there is a surge of methylation part of it attaches to cytosine, one of the four nucleobases of DNA. The imprint of the pain is now part of the DNA and blocks the expression of various genes. Concurrently, methyl and acetyl groups attached to the histones (protein structures which allow the DNA to coil up) may interfere with the timely coiling or uncoiling of the DNA. This disrupts the proper expression of certain hormones and other neurochemical processes. That is part of the reason it is so easy to confuse genetics with epigenetics: our moods and personalities are shaped early on, so we believe psychological disorders are passed down through the bloodlines. After all, if both the parents have blue eyes, it is not a mystery that their child also has blue eyes. 

 But when it comes to behavior and feelings, it is another matter. Controlled by the epigenome, genetic expression can be restricted through experiences the fetus undergoes while in the womb. And it is here that some of the mystery of cancer may be uncovered; for it may be that cancerous cells would evolve as normal cells if not for the physiologic force of repression provoked by maternal stress. This creates lifelong chronic stress in the offspring. It may be that as benign cells surge forward along preordained pathways, they are blocked from their destinations. They are then “crushed” or deviated and can no longer be themselves; they lose their identity and become lethal. As they are changed, we are changed. (More on cancer in a moment.) What all this means is that by examining our womb-life in detail we can often predict our future: our sexual problems, the possibility of later cancer, psychosis, heart problems, Alzheimer’s disease, and a whole host of afflictions (Johnstone & Baylin, 2010). 

 One study suggests that the biological underpinnings of bipolar affective disorder are not primarily genetic, but are epigenetic (Rutten & Mill, 2009). Even an individual’s tendency toward violence, once thought to be a brain disorder, is being shown to have epigenetic roots. In research with rats, investigators at Switzerland’s Ecole Polytechnique Fédérale de Lausanne found that animals subjected to trauma in childhood showed changes in two parts of the brain – the orbitofrontal cortex and the amygdala (Márquez et al., 2013). Those changes taken together combined to lower the threshold of aggressive impulses and weaken the ability to control them. (A report summarizing the findings was also released by the Swiss research university under the title, “Childhood Trauma Leaves its Mark on the Brain.”(2) The results were surprisingly similar to changes found in the human brains of traumatized children who grew up to be violent adults. In addition, the scientists also measured changes in genes known to be associated with aggressive behavior. Here, they found that the psychological stress experienced by the rats caused an alteration in the way these genes were expressed, specifically an increase in the level of MAOA gene expression in the prefrontal cortex, according to Prof. Carmen Sandi, head of the Swiss school’s Laboratory of Behavioral Genetics and director of the Brain-Mind Institute. Researchers were able to reduce the levels of aggression with antidepressants, specifically an MAOA gene inhibitor. In short, childhood stress produced epigenetic changes that heightened violent tendencies. Drug treatment later tamped down the violence, reversing the long-term impact of early trauma. In our own work, we have found that the deeper patients descend down the levels of consciousness the more likely there can be rage and violence. 

 Until recently, the role of epigenetic mechanisms in transmitting trauma across generations has been demonstrated in animals but not in humans. A new study, involving Holocaust survivors and their children, shows for the first time how the epigenetic impact of stress, the cellular changes, can also be passed down among humans, from one generation to the next (Yehuda et al., 2015). Researchers found that children of Holocaust survivors frequently gave birth to anxious children. At first, they thought it was because the parents told horrible stories to the children, but later they discovered that the anxiety came down through the genetic chain, as we shall see in more detail shortly. The point is that the genetic effect of wartime stress had descended from the mother’s physiology through epigenetics. (More on this study in a moment.) 

 I will discuss the clinical implications of the research in the second half of this article. Suffice to say for now that pharmacological treatment may not be the only way to reverse epigenetic changes. We propose that the effects of methylation – as an agent of repression – can be reversed during Primal Therapy, which revisits and resolves the traumatic events that triggered the repressive chemical process to begin with. The real revolution lies in the possibility that people no longer have to live with their genetic inheritance but can actually take charge and change it through Primal Therapy. We believe we may have the method for reversing the long-term deleterious effects of epigenetics, and we are undertaking new research to study that point. If it is life experience that caused changes in the biochemistry and neuronal circuitry, then it is not a fixed entity. It can be altered; the way this is done is by retrieving and reliving key imprints, as I will explain. Heredity is irreversible, but epigenetics is not. It is reversible, which is something I propose we have been doing for almost 50 years. 

 (1) McDevitt, N. (2006, Fall). The nurture of things. Headway. Retrieved from http://www.mcgill.ca/research/files/research/headway-fall-06.pdf 
 (2) Childhood trauma leaves its mark on the brain. (2013, January 15). Ecole Polytechnique Fédérale de Lausanne. Retrieved from http://www.sciencedaily.com/releases/2013/01/130115090215.htm

Epigenetics and Primal Therapy: The Cure for Neurosis (Part 2/20)

Heredity Turned on its Head

Let’s make sure we understand this notion of epigenetics because in the coming years it will likely be one of most important areas of scientific research. As I’ve mentioned, one reason for its preeminence is that many of the serious diseases we think are genetic are actually epigenetic and, therefore, environmentally caused, and possibly treatable. That is now an established fact in human development. However, early discoveries in the field a short decade ago were so startling that they even surprised the scientific world.

The power of epigenetics was demonstrated early on in an experiment at Duke University. That study showed that when female mice were fed a diet rich in methyl it completely altered the fur pigment of the offspring; in other words, it acted like a genetic inheritance when it was not. It was the result of experience, something totally unexpected in the field of genetics until then. As a result of this study, two leading scientists from Canada, Michael Meaney and Moshe Szyf, thought: if that is true why shouldn’t it be true of other experiences such as bad mothering or negligent parenting? (3) Well,it was,and epigenetic research exploded. Think of that: traumatic events in very early childhood leave a mark or tag on a gene that affects us just about forever. That is what I refer to as the imprint, the psychological stamp engraved by harmful events during gestation and early infancy, and burned into the system for life. We now understand that the imprint is aided and abetted by the process of methylation, in which the chemical methyl group is added to the genome to restrict its expression. In other words, the imprint is laid down, in part, by a change in the cell, as certain chemical reactions are taking place — hydrogen removal, methyl infusion, and so on. Methylation leaves a heritable imprint, one that can be passed down even from grandparents to their grandchildren, as research has shown. So what we always thought was genetic may well be the result of very early experience diverting the genetic legacy. In short, the experiences of our forbearers can endure and be passed down the epigenetic chain – the inheritance of acquired characteristics. This is something science thought impossible not long ago.

In another key experiment, the McGill genetics researchers compared two groups of rats: one group consisted of the offspring of normal mothers who frequently licked their babies but had subjected the offspring to stress during pregnancy, with a second group of pups who were also under stress but experienced no licking (Meaney, Aitken, Bodnoff, Iny, & Sapolsky, 1985). Not surprisingly, those babies who were heavily licked turned out to be the most normal and well adjusted. What is a surprise, however, is how much womb-life counts; what the scientists found is that the right amount of licking and grooming early on, left offspring less responsive to stress hormones as adults. It is what we all know: that early love makes us stronger and less anxious. But it turns out that if the mothers were licked and groomed early on in their lives, that experience could be passed on too; the stress hormone genes of their offspring could be modified by the methyl group (and also other chemicals) in a beneficial way. Good history in the mother, good childhood for the children. The more loving by the mother, the less methylation in the child. As we will see shortly, loving in the womb means receiving proper nutrients, being calm and not furiously running here and there, avoiding dangerous or unhealthy situations. I know of someone who did extreme heat/massage therapy while pregnant, never realizing the possible harm to the baby.

Almost every animal form that is loved and licked has grown up pretty healthy with no serious disease; and in my therapeutic experience, those children who had bad and traumatic births with unhealthy gestations are the ones who suffer the most as adults. Too often, catastrophic early life equals catastrophic disease later in life.

To make sure that these changes in the rat pups resulted from experience and not heredity, the researchers let normally stable rat pups raised by attentive mothers be raised by neurotic negligent mothers. And the result was still the same – unstressed babies. These babies had birth mothers who had normal amounts of methylation in their genomes. Thus rats raised by loving mothers could pass it onto offspring even when the adopted mother was not loving. The genes for stress hormone output had minimal methylation; in other words love was passed down the genetic chain. So normal babies raised by negligent and inattentive mothers still had low methyl levels in their hippocampus. The babies started life one leg up; a good start in life despite a bad childhood.

For animal mothers, licking is tantamount to hugging and caressing in humans. And, just as we see in the rats, a woman who is unhappy or depressed while carrying can influence that child for a lifetime, even if she later normalizes and feels better. I believe that changes in the genes, methylation and acetylation, must occur very early as the whole neuronal system is evolving. So before we can state what causes depression or anxiety, we need to observe the early epigenetics at work. Again, pups born to bad mothers but reared by loving mothers still seemed to be normal and relatively un-methylated.

Here is one more reason this research is important: the scientists found that unloving mothers of rodents caused methylation of the estrogen receptors in female offspring. Then, when they had offspring of their own, the offspring were deficient in estrogen, which made them less attentive and loving to their own babies. We as yet do not know how many key chemical processes can be affected by lack of early love, and more, we have no idea how many hormones are changed in neurotic (heavily methylated) mothers, and how that affects myriad adult behaviors.

Nowadays, there seem to be constant breakthroughs in epigenetics research. As I stated at the start, researchers have established that epigenetics is at work not just in animals but among humans as well. In the aforementioned study of Holocaust survivors, published in August in Biological Psychiatry, an international team of researchers led by Rachel Yehuda, professor of psychiatry and neuroscience at The Mount Sinai Hospital in New York, examined the genes of 32 Jewish subjects who had suffered some level of trauma during World War II. They were either held in concentration camps, tortured or forced into hiding. Researchers also examined the genes of 22 adult children of these traumatized survivors. The results were then compared with a control group of Jewish families (eight parents and nine offspring) who were living outside of Europe during the war.

Investigators focused on a specific gene, FKBP5, which is known to
regulate the stress hormone system and determines how well a person handles
stress, according to Elisabeth Binder, director at the Max Planck Institute of Psychiatry in Munich, who directed the molecular analyses. The study found that the war trauma had altered the methylation levels of a specific site within that gene (bin 3/site 6) in both the Holocaust survivors and their offspring. The methylation levels at that site were higher in Holocaust survivors compared to the control subjects. In the survivors’ adult offspring, paradoxically, the methylation levels at that same site were lower, compared to controls. Still, researchers determined that “methylation levels for exposed parents and their offspring were significantly correlated.”

The research has quickly led to a practical, real-world application. In August, around the same time the study was released, London’s Guardian newspaper reported that Jewish activists in Scotland had launched an effort to help the grandchildren of Holocaust survivors suffering from depression, anxiety, addiction and eating disorders. The article makes note of epigenetics studies that document “the intergenerational effects of the Holocaust” by showing that “the atrocities altered the DNA of victims’ descendants.” Armed with that knowledge, activists called for “a mental health provision to treat inherited trauma.” (4)

Although critics say the number of subjects in this study is too small – reflecting the small number of Holocaust survivors still alive – the connection is clear. "The gene changes in the children did not appear to be mediated by adversity experienced during their own childhood but could only be attributed to Holocaust exposure in the parents," said Yehuda, in a statement from the Max Planck Institute (5). "Environmental influences such as stress, smoking or diet can affect the genes of our children.”
In other words, even before a baby is conceived, his genetic destiny is being determined, at least in part, by the life experiences of his parents, not just their existing genetic code. That is epigenetics in action.



(3) Hoag, H. (2011, Summer). Are your genes your destiny? (Not if your mom has anything to say about it). Retrieved from http://publications.mcgill.ca/mcgillnews/2011/06/01/are-your-genes-your-destiny-not-if- your-mom-has-anything-to-say-about-it/

(4) West, J. (2015, August 3). Holocaust survivors' grandchildren call for action over inherited trauma. The Guardian.

(5) Holocaust survivors pass on trauma to their children’s genes. (2015, August 25). Retrieved from http://www.mpg.de/9375728/holocaust-trauma-epigenetics
   

On Developing Cancer and How to Stop It

There is exciting new research taking place on this serious disease.  And obviously, it has to do with epigenetics.  What epigenetics really comes down to is experience.  What kind of experience do we have and when? Because that is the harbinger of serious disease later on.

There is so much new research that points to gestation, pre-gestation and birth trauma as heavily influencing the advent of afflictions such as cancer and Alzheimers later in life.

We know now that one of the key ingredients for this change is a process called methylation. Genes borrow part of the methyl group and change their own evolution; making some more expressive and active, while others are repressive and passive or inactive.  And this depends on what experiences the baby has from the very start of life.  And there may be a similar mechanism that is behind many types of cancer, and dementia, as well. Catastrophic diseases get their start early in life when cells are rapidly forming; and the fact of a catastrophic disease often indicates a catastrophic and life-endangering trauma.  In an era when cells are coming into life is the time when bad events can detour and damage them. Damage during this time can be life-endangering, engendering  diseases that become life-endangering, themselves.  These diseases, therefore, often foretell of severe trauma very early on. They are like measuring gauges that point to times of deleterious effects.

It is not cancer that damages adult cells; these cells already underwent trauma and were weakened by it. Adult stress finishes the job.
The same may be true of heart disease and other common maladies. The on and off changes produced by methylation may be a major element in any number of cancers. One obvious reason is that the cells have been altered in radical ways by this methyl process. So what seems normal to us adults may not be normal at all. Our changes occurred so early that they now seem like “us.” And the doctor examining us asks, “Have you undergone any serious trauma in you life,”  and you say, “Not at all.”   You feel normal as an adult even when you became someone and something else before you had a way of knowing anything.  That is why we can suffer from chronic serious allergies after living a womb-life where the parents were constantly bickering.  “Tell me did you have any serious trauma in your life?"  "No not at all." Alas, the symptoms are screaming the contrary.   And asthma is explaining it all in its own language.

We began a cancer and Alzheimer’s study with a medical clinic which did begin to point to early trauma, but for a variety of reasons we could not complete it.  The point is that epigenetics can either favor cancer development or abort it.  Our future study will be to see if our therapy by demethylating trauma can block the trajectory of deformed cells before they become lethal.  My hypothesis is that it can, but we will see. This means that early damage, a mother smoking or taking pain-killers, can imprint  a cell change, which, when allowed to go on can result in disease.   Altering the epigenetics will right the system and stop the detour.   Voracious cancer has been awaiting its chance; we are not going to let that happen. We already see that in the very few cases of cancer we have among our patients. And I believe it is because in our therapy we travel down to the far reaches and depths—the antipodes-- of the brain where serious illness starts its life.

I recently wrote that parents don’t have to do anything to hurt a child; what they exude (tension or depression) can do it all.  This is especially true during our womb-life where depression and/or anxiety can “exude” from the placenta to affect the baby.  He is being “spritzed” with all kinds of chemicals which affect his development.   And in those "spritzes" are elements that are associated with cancer in later life.  (March 27, 2014  Univ. of Calif. Davis)

Tell me, “did you have any trauma?   Nope. That early trauma does enormous damage; more than almost anything we can think of in our adult life.  If you ask that question in a different way, as we do, and examine primordial events to the fetus, we may find an answer.  As the fetus develops, the mother is informing her baby about herself;  is she depressed, anxious, tense, worried, apprehensive?  That information, seemingly benign, impacts him and affects his evolution and personality.  She doesn’t have to act “nervous.”  The chemicals will do it for her.  But the baby imprints “nervous,” and we wonder where it all came from.

When the carrying mother is nervous she chews up her vitamins; the baby needs those vitamins to synthesize methyl groups.  So when the mother is deficient, so is the baby. And that again can change everything. It is becoming more and more clear, as I have insisted for almost 50 years, that our early life is critical; that problems in the womb redound in later life and account for so many illnesses.  The real question by doctors should be, “Tell me about your gestation and birth. Tell me about your parents during that time.”

The Mystery Known as Depression, Part 5/12

5. THE KEY ROLE OF EPIGENETICS

Although genetics may be partly responsible for depression in rare cases, by and large it is early life experience (including experience in the womb and birth trauma), that is the root cause. What we see at work is epigenetics, the altering of gene function without changes in the underlying DNA sequence (Booij et al., 2013). Those alterations, or deviations, if you will, often involve a biochemical process known as methylation. And it is through methylation that psychological trauma is imprinted. Thus the trauma – which can be as simple as a lack of caring and love by the mother – becomes “fixed” in the system and endures. It is the imprint, the linchpin of depression. The biochemistry, and ultimately the brain have been rerouted, sealing in depressive tendencies. It is this imprint that ultimately must be addressed and resolved.

What the scientific evidence shows more and more is that gestation and birth events are critical for later disease. In a 2010 study conducted at the Hannover Medical School in Germany,researchers concluded that “epigenetics is of considerable interest for the understanding of early life stress in depression.” The study, published in the journal Current Opinion in Psychiatry, found, among many other things, that unloved and untouched children had a predisposition to depression. (Schroeder, Krebs, Bleich, & Frieling, 2010). Recent work by a team of Canadian researchers also pointed to the critical role played by epigenetics. (Booij et al., 2013) 
The following passage is from their article:
“The functioning of the hypothalamic–pituitary–adrenal (HPA) axis and serotonergic (5-HT) system are known to be intertwined with mood. Alterations in these systems are often associated with depression. However, neither (is) sufficient to cause depression in and of themselves. It is now becoming increasingly clear that the environment plays a crucial role, particularly, the perinatal environment. In this review, we posit that early environmental stress triggers a series of epigenetic mechanisms that adapt the genome and program the HPA axis and 5-HT system for survival in a harsh environment. We focus on DNA methylation as it is the most stable epigenetic mark. Given that DNA methylation patterns are in large part set within the perinatal period, long- term gene expression programming by DNA methylation is especially vulnerable to environmental insults during this period. We discuss specific examples of genes in the 5-HT system (serotonin transporter) and HPA axis (glucocorticoid receptor and arginine vasopressin enhancer) whose DNA methylation state is associated with early life experience and may potentially lead to depression vulnerability. We conclude with a discussion on the relevance of studying epigenetic mechanisms in peripheral tissue as a proxy for those occurring in the human brain and suggest avenues for future research.”
It seems that the fastest changes in methylation occur early in our lives, at the very least in the neonatal period, though this thesis is subject to further study. What is important now is that certain genes which should not be silenced, are. Thus, certain means of expression are suppressed, which is often the case in depression. None of this means that methylation “causes” the affliction but rather, there are adverse events very early in life that increase its production.

Though the Canadian researchers emphasize the perinatal period, we have found the imprint to lie earlier, as well. If the neonate is especially sensitive to environment insults, it surely is possible that those insults can occur earlier and form the primordial imprint that later gives rise to depression. Methylation, in brief, offers the primordial event that sets the prototype for later inhibition and repression; thus, high methylation may be a predictor for later depression. It means that certain key genes which should find expression are silenced, especially due to modification of the genes promoter region. The tendencies for no or difficult expression are imprinted.

My opinion is that some of these changes in physiology occur during our life in the womb, when the set-points of so many hormones are being established, including thyroid hormone. Indeed if we give a small does of thyroid medication to depressive patients there is a transient improvement. One may think that such deficiencies are genetic but there are events that can cause them that are not always obvious. They are only obvious when the patient in therapy descends down to the far reaches of the unconscious where the crucial explanation of one’s depression lies. One again relives the birth experience, the suffocation, strangulation, the hopeless battle to get out – the unutterable and ineffable despair. Of course, it is not given a name until years later but the feeling is there engraved in the nervous system. We can feel hopeless without giving it a label. In the face of adult adversity, the old imprint – wanting to give up – appears and is now called depression.

We give it that name because we have not seen the generating sources of deep imprinted despair, something we have observed many times. We name it depression because we do not know the hopelessness inside that makes us miserable. We give depression the name of the defense instead of its cause – pain.

Epigenetics and Primal Therapy: The Cure for Neurosis (Part 16/20)

(After a long pause, I will be publishing the remaining articles about Epigenetics and Primal Therapy over the next few days.)

How Early Is Too Early?

In the scientific community, the question has always been, “How early is too early?” And this is where epigenetics is relevant to our discussion. A group at Washington State University led by Matthew Amway found that gestational experience in animals that sways the genetic unfolding can show effects for three generations. They found that exposing pregnant adult rats with defective sperm could engender many diseases, including cancer, in adult animals. Females avoided mating with other rats that were also exposed during gestation. And this went on, not only for the life of the adult, but for the life of their offspring, as well. It seems that the system knows how to behave given certain biologic deficiencies, and it does so according to what is best for heredity, what gives us the best shot of succeeding in life. So when we cannot explain some trait in adults by heredity we may have to reach back several generations to find the answer we’re looking for. This gives us a new perspective on so-called psychological problems in adults. When we do an intake interview of prospective patients, it has to be thorough enough to include the prenatal life of the patient, as well as their parents and sometimes the grandparents, as well.

Without clinical evaluation we can only guess as to what traumas may have occurred in the life of a pregnant mother, and what adaptations continue to show their effects in her children and grandchildren. Of course, it isn’t just that a mother underwent trauma, but that the trauma has altered her basic physiology and produced lifelong changes in her and her offspring. Did the pregnancy occur in wartime? Were the parents fighting all the time? Was the child’s grandmother depressed? Was she a heavy smoker or drinker during her pregnancy? These are all questions we should be asking.
And in truth the distinction between heredity and epigenetic “heredity” must be made, if we are ever to reverse disease. When a mark is made on certain anxiety-regulating cells, for instance, we may be stressed until that mark is revisited and relived. As I have noted, the process of methylation also can be chemically reversed by demethylation agents, for example. That leads us to believe that certain regions of the brain altered by drugs are the same areas that may be affected by reliving gestational events.

What is most important is that stress in the mother compromises the repressive system in the fetus, so that later it will be difficult to mitigate surging feelings. Low-level imprints from womb-life burst through the repressive barrier, overloading the system, and — in the absence of a cohesive cortex — result in difficulty focusing and concentrating, and problems learning. The prefrontal cortex becomes overwhelmed as it is pressed into service to counteract and hold down painful feelings.

Why are those early imprints so critical? Because almost every key adverse event in the womb can be life-endangering: low oxygen, inadequate nutrition, too much agitation, flooding by drugs or alcohol, etc. they all affect vital organs and change the system of the baby accordingly. I will never omit smoking, which is deadly to the maturation of the baby. Imagine being in the womb while a mother ingests all kinds of toxins hour after hour, every day of the year. Who can survive that?

There is a beginning to personality development and we must not immediately ascribe it to genetics. Epigenetics is possibly more important. Life circumstances wrap themselves around the gene, and alter who we are and what we become. It is those days in the womb that form the crucible for personality type; they all accommodate life circumstance. They pivot around the imprint; and when we take patients down deep we find the little nugget, the key imprints that forced all that accommodation. And when those early imprints are relived and all the vital signs move as an ensemble down lower, we know we have struck gold. We have found Nirvana, the core of the pain. Remember, there is no suffering in the pure state of Nirvana.

What is New About the Imprint?

It seems that new research is confirming much of the Primal position. This is especially true of the work of Michael Meaney and Moshe Szyf (McGill University,Canada). (see for example http://publications.mcgill.ca/headway/magazine/the-nurture-of-things/ or http://publications.mcgill.ca/mcgillnews/2011/06/01/are-your-genes-your-destiny-not-if-your-mom-has-anything-to-say-about-it/ or http://epigenome.eu/en/2,68,1181 ) They are critical work on epigenetics, and how imprints through methylation can be passed down from one generation to another.

They don’t call it an imprint but that is what it is……a key repressed memory that endures and persists throughout our lives; it drives behavior and symptoms. It turns out that imprints can be passed down from parents to baby and from grandparents to baby. Methylation depends on the work of the chemical methyl group which is recruited when there is a traumatic event, and helps embed that memory. . It seems that when there is a surge of methylation part of it attaches to one element of the gene known as cytosine. It is now part of the DNA and turns on or off certain hormones and other neuro-chemical processes.. Once that happens methyl is recruited and the genetic unfolding is thereafter altered.

In short, methylation can be an agent of repression. A study at Duke University showed that when female mice were fed a diet rich in methyl it completed altered the fur pigment of the offspring. In other words, it acted like a genetic inheritance when it was not. It was the result of experience and that is the linchpin of our theory… epigenetics.

As a result of this study the two scientists from Canada, (Meaney and Szyf) thought, if that is true why shouldn’t it be true of other experiences such as bad mothering or negligent parenting? Well, it was and epigenetics research exploded. Think of that: traumatic events in very early childhood leave a mark or tag on a gene that affects us just about forever. They found that even grandparents affected the imprints of the grandchildren, which we will get to in a moment. But suffice to say that the experiences of our forbearers can endure and be passed down the genetic chain, the inheritance of acquired characteristics. This is something science thought impossible decades ago.
 What the scientists found is that the right amount of licking and grooming early on left offspring with less chronic stress hormone output as adults. It is what we all know; that early love makes us stronger and less anxious. But it turns out that if the mothers were licked and groomed early on in their lives, that experience could be passed on. The genes could be modified by the methyl group (and also other chemicals) in a beneficent way. Good history in the mother, good childhood for the children. And more loving by the mother the less methylation in the child . And with less chronic stress hormone production there is far less chance of serious diseases later on such as Alzheimer’s.

To make sure that these changes in the rat pups resulted from experience and not hereditary, they let normally stable rat pups be raised by neurotic negligent mothers. And the result was still the same,; unstressed babies. These babies had mothers who had normal amounts of methyl in their systems. Thus rats raised by loving mothers could pass it onto offspring even when the adopted mother was not loving. The genes for stress hormone output had minimal methylation. In other words love was passed down the genetic chain. So normal babies raised by negligent and inattentive mothers still had low methyl levels in their hippocampus. The babies started life one leg up, a good start in life despite a bad childhood. I believe that changes in the genes, methylation and acetylation, must occur very early as the whole neuronal system is evolving. So before we can state what causes depression or anxiety, we need to observe the early epigenetics at work. Again, pups born to unloving mothers were handed over to loving mothers, and those born to bad mothers reared by loving mothers still seemed to be normal and relatively un-methylated.

Here is one more reason this research is important: they found that unloving mothers of rodents causes methylation of the estrogen receptors in female offspring. Then when they had offspring of their own the offspring were deficient in estrogen which made them less attentive and loving to their own babies.  We as yet do not know how many key chemical processes can be affected by lack of early love. And more, we have no idea how many hormones are changed in neurotic mothers (heavily methylated) and how that affects myriad adult behaviors. Is depression inherited? There may be precursors for it which is never manifested if there were plenty of love later in childhood. Is some of the tendency to methylation inherited or epigenetically passed on? And does that form the basis for depression? It seems from the research just cited that that neurotic mothers (methylated), are ineluctably forced to be unloving, thus laying the groundwork for depression in the offspring later on. And what other hormones are depleted by this scenario? Are we born with a tendency to anxiety? Possibly but then the imprint is not methyl so much as acetyl., in this case. With acetylation there are more faults in the repressive system and “holes” in the gating system. Acetylation (recruiting acetyl) pretty much produces the opposite of methylation, a tendency to open rather than close.

Early trauma produced heavy methylation in those children who grew up in orphanages. And that process then affected much more in terms of brain and neuronal development. So when we find a mother who is not loving we need to know that she may being driven by her epigenes; she is a victim of those changes. Her cortisol/stress hormone level militates against maternal instincts. Methylation shuts down a number of “natural” behaviors. In neurosis we cannot be natural and appreciate nature because we are disconnected and alienated from our own nature.. We cannot rely on our feelings to guide us because they have effectively been shut down; we are alienated from them. Literally, the feelings are aliens. We have found that patients on the verge of these feelings in sessions often run a fever. The body treats the feelings as a menace, a danger and something to be avoided; yet it is also what can liberate us.

Can we reverse or undo methylation? The research informs us that with rats who had been damaged, and raised by unloving mothers, when they were infused with trichostatin did not show evident damage. As though the trauma never occurred. This drug removes methyl from the system. It did, in brief, undo history. This is what I think may be happening with our patients. In the reliving there must be a change in methylation so as to reverse history; this is what we shall study in our future research projects. It seems to me the natural way provides far less possibility for collateral damage to the system. Since we already have found that chronically high cortisol levels have been reversed in our therapy, it would perhaps follow that methylation could also be reversed. In a way, the levels of methylation can be a marker for having been loved early on or not having been loved. We could tell more than the statements by the person who claims he was loved in his childhood if he were indeed not loved. How much denial is there?

Neurochemistry may be better relied on because it has no reason to lie and wouldn’t know how to do it even if possible. It can be a marker for post traumatic stress or how much repression exists in ADD. Or how much pain/repression is there in Alzheimer’s disease? We already have some information in this regard because autopsies on depressive/ suicides found them to have been heavily methylated in the hippocampal area. The more abuse as a child in these cases the more methylation produced. When we add this to our future research on telomeres and cortisol we will begin to have precise measures of the pain in us. And we will know when a drug is too dangerous for us, particularly the drugs like marijuana that tend to open us to ourselves; to our feelings and pain. Finally we will have a marker for the efficacy of certain psychotherapies.  Does the therapy undo the past? Does it help relieve repression and therefore depression? Is there great first line pain in anxiety states? What seems to be the case is that love obviates methylation and produces normal souls.

Epigenetics: The Inheritance of Acquired Characteristics

There is something we must immediately add to the theoretical mix: epigenetics; how very early events in the womb and at birth can alter the genetic unfolding. One genotype, a single genetic predisposition, can give rise to many phenotypes depending on what happens to those genes during gestation. So what we might imagine is genetic, is genetic-plus what happens to us in the womb. I was so surprised early on in my therapy when long-term patients reported that their wisdom teeth descended. Now I understand it better; the genetic unraveling toward its destination was deferred due to repression.

In the early nineteenth century, a French scientist named Jean Baptiste Lamarck decided that we acquired characteristics from experiences that our parents underwent. Russian communists applied this to agriculture but, no matter, it was a widely discredited theory … until recently. Now this avowed Marxist position may have been resurrected a bit. There is a new field called epigenetics that states pretty much what Lamarck believed. So what is the evidence? And what exactly is it? What Lamarck said was that individuals acquire characteristics as a result of their environment, and now, these characteristics can be passed on to the offspring.

Much of the work in epigenetics has to do with diet; a mother’s diet influences the offspring’s physiology. Epigenetics has to do with how genes are regulated and influenced by the experience of the baby. I believe it has more to do with the fetus who resides in the womb; that his experience is influenced forevermore by the mother’s diet but also by her moods.[1]


Has the genetic switch been delayed or was it premature? This can happen without making a radical change in the gene itself but rather in how it is expressed, whether it is shut off or on. What we are discussing is how a mother’s interaction with her environment can pass this on to her offspring. I think we need to understand that a fetus in the womb is always trying to adapt to his environment and that his genes will evolve and be expressed depending on that adaptation. For example, a mother who is very unhappy from her own childhood pain, and who has depleted much of her serotonin supplies cannot fulfill the young fetal need for his own serotonin supplies. (His own supply does not kick-in until somewhere around the half-way mark). He may well grow up deficient in inhibitory or repressive capacity and be an anxiety/impulsive case forevermore; this can evolve into attention deficit in his youth. This will happen when the fetal set-points are readjusted because of events during womb-life. There may be a continued inability to have a cohesive cognitive ability; to focus and concentrate. I think it is important that all this occurs while the fetal brain is rapidly developing and needs proper input to evolve normally. An anxious mother is so agitated that the neuronal input into the baby she is carrying is so extreme that he cannot adapt and integrate this input. Thereafter, this is the kind of person who cannot accept too much stimulation because the internal input is so great that anything from the outside, such as two term papers due immediately, can be overwhelming.

To get an idea of how early all this may begin, there is a study by the University of Miami School of Medicine that states that: “A review on (maternal) prenatal depression effects on the fetus and newborn suggests that fetal activity is elevated, growth is delayed, low birth weight common.” [2] It begins a lot earlier than we previously thought. As if to underscore this position, there is a study from Scientific American Mind, (Fetal Recall. January 2010)that is seeking out when consciousness actually begins. And they are quoted as stating that it begins in the womb. They introduced sharp sounds to the pregnant mother (a honking device placed on her abdomen). As they did it the fetus reacted significantly. But after a time the fetus stopped responding to it (Squirming. Heart rate stopped speeding up). He became habituated, got used to it, and it remained, therefore, as only a memory. He “learned” that the noise was no longer dangerous. And the memory endured.

Newborns of a depressed mother show a profile that mimics the mother’s prenatal state, including her physiologic state; this includes higher stress hormone levels, lower levels of dopamine and serotonin, and greater right frontal brain activity. What I think this means is that the right/feeling brain is forced to be hyperactive to deal with emotional push. It is, after all, the right prefrontal brain (orbitofrontal area) that maintains a history of our feelings and has a more internal focus. To summarize: Higher resting levels of stress hormones in the carrying mother can already have an effect on the later life of the offspring. It already presages the constant need for tranquilizers because the early imprint has lowered levels permanently. Then with even minor setbacks later on, the resonance factor can compound the pain level so that taking painkillers is a matter of urgency.

The concept of epigenetics has import for diagnosis. For example, one of my patients was told that she had a genetic vulnerability, very much like her mother had. It led to a diagnosis of a “very serious autoimmune disease.” If it were seriously genetic, as the doctors believed, then any chance to change her state would be close to nil. What this does is prevent us from seeing or investigating beyond the inheritance to factors that may have been equally important; what happened to the baby while being carried? Further, if there were something that altered the immune state while in gestation, perhaps one can relive and connect to it, thus affecting that imprint. Thus, it may be as a result of an experiencerather than inheritance that is ultimately significant. This patient did relive her traumatic birth, and, perhaps, that helped her make some progress against the disease. This happens, again, because in reliving, it is possible to gather up associated feelings and sensations that lie even below the later trauma but which may be related to it through frequency resonance. Reliving later events will usually bring up the earlier events and feelings that it resonates (triggers off) with. Earlier imprints will be re-represented on higher levels as the brain develops. Even though we are reliving something at the age of sixteen we are also dealing with the earlier part of the related feeling. That is why there is hope when we relive; we can attack imprints during gestational life. So when a feeling event brings up severe anxiety with it, it can mean that we are basically dealing with preverbal events where and when anxiety/terror is installed. The importance of differentiating between genetics and epigenetics is that we may be dealing with a reversible disease, not one that is inherited and cannot change. And indeed this is already being tested. In a paper by M. Szyf, (Dept. of Psychiatry, McGill University, Quebec. “The Epigenetic Impact of Early Life Adversity.” He reported on the reversibility of the epigenomes in animals. Using chemical agents they were able to reverse the changes caused by epigenetic events. This has great import for disease today; for certainly there may be genetic factors which only become manifest when certain traumas occur, but even after they occur we may be able to go back and change it. Hence reverse disease. Terribly important.

Researchers at Karolinska Medical Center, Sweden, have found that cesarean births can result in increased allergies, diabetes and leukemia risk. Mikael Norman states: “Our theory is that altered birth conditions could cause a genetic imprint in the immunecells that could play a role in later life.”[3] Their work, as is that of others, indicates that stress around birth affects the genes. The assumption is that the fetus is not prepared for an “unnatural” birth. It is different from a vaginal birth where the stress gradually builds and can be adapted to.

There are experiments with pregnant primates. As a result of stress during pregnancy there is an adverse effect on the hippocampus (dealing with memory). It seems to shrink. And, as I have mentioned elsewhere, one has to wonder if this kind of stressful gestation can play a role in later Alzheimer’s. There is new evidence on this point: a study by Brigham Young University found that the size of the hippocampus was reduced when trauma occurred. (Neuroscience, Aug. 2009. See also, “Trauma, PTSD, Followed by Reduction of The Brain Involved with Memory.” Science Daily, Aug 27, 2008). It took a long time to discover this because there was no immediate damage; only after a long period did the damage show up. More importantly, again, there is no taking into account the unobserved trauma in the womb and at birth which, in my opinion, does permanent damage to the memory centers. It is not just an assumption; there is new research to demonstrate this: in a paper (reported in Science News, Jan. 4, 2010. “Acute Stress Leaves Epigenetic Marks on the Hippocapus), there is more and more evidence of this. A single trauma in rats can produce changes in their brains, and these changes are reflected in the memory centers such as the hippocampus. The changes that occur can also affect whether or not our genes are turned on or off. It is so difficult to differentiate between nature and nurture as causes because they are so intertwined as we mature.

A corollary of this is that as stress increases so does the mother’s level of cortisol. That, in turn, affects the brain structures. The investigators indicated: “If there is anything we all agree on it’s that the fetus is incredibly vulnerable and fragile, and that even subtle perturbations in the mother’s mood can have measureable effects on the fetus that last for years.”[4] One additional finding. Stress while being carried, later lowers IQ, as well as anxiety, ADD and depression.[5]

The thalamo-cortical circuits are finally established very late in gestation (thalamus to cortex and back). When amygdala-cortical circuits are in place it is then possible to have a mental appreciation of the pain we are in. It is before thalamic and amygdaloid circuits are mature that we can experience pain without acknowledging it. Thus pain can be laid down in a completely unconscious way, and most certainly there are no words to clarify or explain it. Can one imagine getting a patient to explain a gestational trauma? But he can describe a sensation of butterflies in the stomach, pressure on the chest and a churning sensation in the belly. We call it amorphous anxiety but these are part of the overall experience of fear and terror while we are being carried. Each is a fragment of a gestalt experience.[6]

There was a study reported in the British journal, Nature.[7] They noted that when the baby is under threat the amygdala signals to the prefrontal cortex triggering the expression of that fear in behavior. The cortex becomes the “decider.” What the investigators did was to train mice with a tone accompanied with a shock. When that was administered there was commensurate brain activity in the prefrontal area of the mice. But when the amygdala was surgically removed there was no longer any prefrontal activity; it could no longer signal fear to the top level. The same is true when we drug that structure or tranquilize it; it diminishes the force that mounts in the prefrontal area. We see from this research why so many of us have trouble sleeping; either falling asleep or staying asleep. And why some individuals cannot get into feeling. Lower level imprints voyaging or meandering upwards and forwards keep the person from traveling to a lower level of brain function. It literally jolts the person who has lain down for a few minutes trying to relax, into a hypervigilant state. There is too much going in that deeper level to permit entry. Lower level imprints are stimulating the frontal thinking/ruminating neurons to get busy. Thus in quieting the lower levels there is a sense of calm in the thinking area. A false sense, I might add. But the person reports feeling calmer. So much for subjective reports.

So when can a fetus feel pain? A better question might be: when can it signify pain? After the circuits are in place. Neuroscientist J.K.S. Anand explains this when he placed a needle/probe into a fetus (for amniocentesus). The fetus grimaced in pain and its stress hormone levels rose dramatically. The baby suffered; not only that but from our point of view, that suffering can be coded and registered in the memory system, thereafter lying in storage waiting its chance for connection. And this is what we in feeling therapy are about—connection.

There are some serious diseases out there that have been considered only in the domain of inheritance; muscular dystrophy is one of many. Perhaps the cures for these afflictions have been slow in coming because our emphasis has been on inherited factors rather than experience. If we don’t look at gestation as critical, our diagnoses are bound to be skewed.

There is a study by a Canadian group from the Douglas Mental Health University that found when child abuse exists there is a change in a gene (NR3C1) that affects how the child will deal with abuse. That gene was much lower in abuse victims who eventually took their lives. It would seem that childhood abuse had changed the structure of the gene so that it was less active. And these changes endured throughout their lives. It changed the way the whole stress apparatus functioned (the HPA). McGowan implies that the changes are stable and that they alter the gene’s activity leading to later illness and suicidal tendencies. When that gene is ineffective it cannot produce the kind of alerting, galvanizing chemicals that help one fight through things (glucocorticoid hormones). So the body behaves as though it were constantly under stress when there is none apparent. It is reacting to the imprint. What this research group believes is that mothers can affect the fate of their children even before they are born. The epigenetic changes could force the children to be depressed and suicidal later on. It will look like genetics but it will be more than that.

And to make matters worse, there is a study that indicates that a mother who is been stressed before she gets pregnant can also affect the life of her offspring.[8] This was a rat study by the Israeli M. Lesham. Those rats who underwent stress before pregnancy had offspring who were hyperactive. The females displayed symptoms of anxiety and were generally more nervous. In general a nervous mother is not providing a good soil for having children. We then say she is just like her mother. It is inherited. No it is not. It is what that mother does to her baby just by who she is.

Every day there is new information and research on this subject. A new study by Alberto Bucay of the Research Center, Halabe and Darwich, Mexico, is now suggesting that when parents are happy it can change the germ cells (egg and sperm) that will affect the offspring. He writes in Bioscience Hypotheses, reported in Science News,[9] that parent’s psychology and emotional state before conception can affect the child’s genes. For now this proposal is mostly polemical but it is intriguing. It is for all these reasons that epigenetics will soon be a very important area of study, something that did not exist when I was coming up in psychology.



[1] I discuss research into anise later on.

[2] Infant Behavior Development. July 29, 2006. Pgs. 445-455. “Prenatal Depression Effects on the Fetus and Newborn.”

[3] Healthday News. July 09

[4] Vivette Glover. Imperial College, London. Royal Society Summer Science Exhibition. July 9, 2009

[5] See:“Stress During Pregnancy May Lower Baby’s IQ” British research. Reported in the Globe. Canada Zosia Bielski.

[6] “Neuro-developmental Changes of Fetal Pain.” Semin. Perinatol. 2007,
Oct 31,(5) 275-82.


[7] Nov. 18, 1999
[8] Science Daily. May 13, 2009. “Trauma Experienced by a Mother Even Before Pregnancy Will Influence Her Offspring’s Behavior.”

[9] “Can Happiness be Inherited?” May 14, 2009

The Inheritance of Acquired Characteristics: Epigenetics

In the early nineteenth century a French scientist named Jean Baptiste Lamarck decided that we acquired characteristics from experiences that our parents underwent. Russian communists applied this to agriculture but, no matter, it was a widely discredited theory…..until recently. Now this avowed Marxist position may have been resurrected a bit. There is a new field called epigenetics that states pretty much what Lamarck believed. So what is the evidence? And what exactly is it? What Lamarck said was that individuals acquire characteristics as a result of their environment, and now, these characteristics can be passed on to the offspring.

Much of the work in epigenetics has to do with diet; a mother’s diet influences the offspring’s physiology. Epigenetics has to do with how genes are regulated and influenced by the experience of the baby. I believe it has more to do with the fetus who resides in the womb; that his experience is influenced forevermore by the mother’s diet but also by her moods, her anxiety and depression. Has the genetic switch been delayed or was it premature? This can happen without making a radical change in the gene itself but rather in how it is expressed, whether it is shut off or on. What we are discussing is how a mother’s interaction with her environment can pass this on to her offspring. I think we need to understand that a fetus in the womb is always trying to adapt to his environment and that how genes will evolve and be expressed depends on that adaptation. For example, a mother who is anxious and who has depleted much of her serotonin supplies cannot fulfill the young fetal need for his own serotonin supplies. He may well grow up deficient in inhibitory or repressive capacity and be an anxiety case forevermore; this evolves into attention deficit in his youth and his continued inability to have a cohesive cognitive ability. I think it is extremely important that all this occurs while the fetal brain is rapidly developing and needs proper input to evolve normally. An anxious mother is so agitated that the neuronal input into the baby she is carrying is so extreme that he cannot adapt and integrate this input. Thereafter, this is the kind of person who cannot accept too much stimulation because the internal input is so great that anything from the outside, just two terms papers, can be overwhelming.

I have discussed the work of Michael Meaney of McGill University who has worked with mice and found that very early neglect by the mother results in lifelong alterations. In thirteen men who had committed suicide, all of whom suffered from child abuse, there were epigenetic effects. Abuse has many forms but to me those most deleterious is the abuse of a mother who smokes, drinks or takes drugs during pregnancy. Abuse means adversely affect a child’s development. Meaney found the same changes in thirty five people who suffered from schizophrenia. Here, several of the genes involved with the unfurling of key neurotransmitters (which ordinarily help to repress pain or noxious stimuli) where affected. New work has related epigenetics to the occurrence of cancer. What has been called the effects on epigenetic settings I call changing the set-points of many biologic states; this includes the set-points of the neurotransmitters that w
Ill later make us chronically comfortable or uncomfortable. Not feeling good in our skin is one way to state it. What is very new is that experiences of the mother affects the sperm of the offspring, and that may affect how the grandchildren develop. It may be that smoking or drug taking in while the embryo is just forming can later affect sperm production. The meaning of all this is that what happens in the womb while the organism is getting organized can affect the baby for a lifetime. It is so important that we not neglect this period when we attempt to understand and treat those with emotional problems. The more remote the imprint the more widespread the later effects, in my opinion. When a carrying mother is under stress her stress hormone level is high. When the levels remain high for a long time the immune system is compromised, and that might well affect the immune status of the offspring. And as I note elsewhere, a strong immune system (natural killer cells) is needed to stay on the lookout for newly developing cancer cells. It is not that a deficient immune system can lead to cancer, it is that a weak maternal immune system does not impart a strong immune capability to the baby; and the same dislocated physiology of the mother can also affect the fetus, setting the stage for later catastrophic disease. Womb-life has largely been neglected in the psychological literature. It is time to reorient ourselves.

SMALL FEET AND SMALL BREASTS: CANCER?

Are small feet and small breasts desireable? Is it good or bad? It’s more serious than that. It is neither good nor bad but whether that size has arrived at its genetic destination. That is, due to heredity has the size fulfilled the genetic intention? If not, there can be serious repercussions. What it means to me, and now we leave the arena of strict science, is that repression has interceded to slow down or inhibit growth. How do I know? Some of my patients have reported foot growth, chest growth, breast growth and other kinds of growth after about a year of therapy. (We have a letter of a former patient who reported foot growth of several sizes after therapy). All that has happened in my therapy is lifting repression and liberating pain. If we reason backward we might say that repression probibited proper growth from taking place. That means to me constant pressure in key sites against growth; against genetic destinations. And that again can mean the possibility of serious illness, possibly cancer. Pressure on the cells to stop this unfolding can be enormous. Until one has seen the liberation of pain it is difficult to comprehend.

So we can only say that one’s breasts are too small when we see if they grow as a result of this liberation. And I believe that will only happen when the patient arrives at deeply implanted pain, at birth and before, when so many hormones are affected; where so many set-points are dislocated and fixed. I think that, in this sense, the therapy may have an anti-cancer effect. Can you imagine the pressure our biology exerts to fulfill its genetic promise? That pressure continues against a constant pressure to hold it back. The result too often can be disease as the cells become deformed and dislocated. It is not only the obvious breasts and feet, which are, after all, measureable, but there my be so effects we cannot measure; for example, the kidneys, heart or liver. We see that wherever we have looked, (serotonin/impramine: natural killer cells) there are significant changes. We would expect the same with key organ systems. In other words, pain and repression are laid down as total experience, which means that just about every system is involved in the imprint of the memory. So we would expect that all key organ systems would be affected. That remains to be studied. But we would also expect that those systems, which are inherently weak and vulnerable, would be seriously affected by that repression. The answer? Have a good gestation and birth and infancy. Failing that, relive the key pains set down and undo the massive repression.


There are effects we cannot measure; for example, the kidneys, heart or liver. We see that wherever we have looked, (serotonin/impramine: natural killer cells) there are significant changes. We would expect the same with key organ systems. In other words, pain and repression are laid down as total experience, which means that just about every system is involved in the imprint of the memory. So we would expect that all key organ systems would be affected. That remains to be studied. But we would also expect that those systems, which are inherently weak and vulnerable, would be seriously affected by that repression. The answer? Have a good gestation and birth and infancy. Failing that, relive the key pains set down and undo the massive repression.



In writing about the imprint, I will note again that one way we know that very early imprinted pain endures is that many entering patients have high stress hormone levels which normalize after one year of the therapy. What this may mean is that the imprint endures, is a constant danger, and must be fought against. That danger is signaled by the high cortisol (stress hormone) levels. Why is it, then, that the levels come down to normal after a time? Because the imprint is no longer a force; It is now simply a memory. The force of the pain has been felt and integrated. It is not as though there is a reliving of the memory and then we find changes in the imprint; it is that the way the memory is held and engraved is through these various changes such as in stress hormone levels. The danger is no longer in evidence; the system can relax. The battle is over. As all systems normalize it means that there is no longer an irrevocable memory to deal with. The imprint as a total physiologic event no longer exists. Can we become neurotic again? Not in the same way because the harmful memory is gone. What we often cannot change are the secondary changes already in evidence due to the damage inflicted beforehand.

The Inheritance of Acquired Characteristics: Epigenetics

(Originally published July 27, 2008)

 

In the early nineteenth century a French scientist named Jean Baptiste Lamarck decided that we acquired characteristics from experiences that our parents underwent. Russian communists applied this to agriculture but, no matter, it was a widely discredited theory…..until recently. Now this avowed Marxist position may have been resurrected a bit. There is a new field called epigenetics that states pretty much what Lamarck believed. So what is the evidence? And what exactly is it? What Lamarck said was that individuals acquire characteristics as a result of their environment, and now, these characteristics can be passed on to the offspring.

Much of the work in epigenetics has to do with diet; a mother’s diet influences the offspring’s physiology. Epigenetics has to do with how genes are regulated and influenced by the experience of the baby. I believe it has more to do with the fetus who resides in the womb; that his experience is influenced forevermore by the mother’s diet but also by her moods, her anxiety and depression. Has the genetic switch been delayed or was it premature? This can happen without making a radical change in the gene itself but rather in how it is expressed, whether it is shut off or on. What we are discussing is how a mother’s interaction with her environment can pass this on to her offspring. I think we need to understand that a fetus in the womb is always trying to adapt to his environment and that how genes will evolve and be expressed depends on that adaptation. For example, a mother who is anxious and who has depleted much of her serotonin supplies cannot fulfill the young fetal need for his own serotonin supplies. He may well grow up deficient in inhibitory or repressive capacity and be an anxiety case forevermore; this evolves into attention deficit in his youth and his continued inability to have a cohesive cognitive ability. I think it is extremely important that all this occurs while the fetal brain is rapidly developing and needs proper input to evolve normally. An anxious mother is so agitated that the neuronal input into the baby she is carrying is so extreme that he cannot adapt and integrate this input. Thereafter, this is the kind of person who cannot accept too much stimulation because the internal input is so great that anything from the outside, just two terms papers, can be overwhelming.

I have discussed the work of Michael Meaney of McGill University who has worked with mice and found that very early neglect by the mother results in lifelong alterations. In thirteen men who had committed suicide, all of whom suffered from child abuse, there were epigenetic effects. Abuse has many forms but to me those most deleterious is the abuse of a mother who smokes, drinks or takes drugs during pregnancy. Abuse means adversely affect a child’s development. Meaney found the same changes in thirty five people who suffered from schizophrenia. Here, several of the genes involved with the unfurling of key neurotransmitters (which ordinarily help to repress pain or noxious stimuli) where affected. New work has related epigenetics to the occurrence of cancer. What has been called the effects on epigenetic settings I call changing the set-points of many biologic states; this includes the set-points of the neurotransmitters that w
Ill later make us chronically comfortable or uncomfortable. Not feeling good in our skin is one way to state it. What is very new is that experiences of the mother affects the sperm of the offspring, and that may affect how the grandchildren develop. It may be that smoking or drug taking in while the embryo is just forming can later affect sperm production. The meaning of all this is that what happens in the womb while the organism is getting organized can affect the baby for a lifetime. It is so important that we not neglect this period when we attempt to understand and treat those with emotional problems. The more remote the imprint the more widespread the later effects, in my opinion. When a carrying mother is under stress her stress hormone level is high. When the levels remain high for a long time the immune system is compromised, and that might well affect the immune status of the offspring. And as I note elsewhere, a strong immune system (natural killer cells) is needed to stay on the lookout for newly developing cancer cells. It is not that a deficient immune system can lead to cancer, it is that a weak maternal immune system does not impart a strong immune capability to the baby; and the same dislocated physiology of the mother can also affect the fetus, setting the stage for later catastrophic disease. Womb-life has largely been neglected in the psychological literature. It is time to reorient ourselves.

SMALL FEET AND SMALL BREASTS: CANCER?

Are small feet and small breasts desirable? Is it good or bad? It’s more serious than that. It is neither good nor bad but whether that size has arrived at its genetic destination. That is, due to heredity has the size fulfilled the genetic intention? If not, there can be serious repercussions. What it means to me, and now we leave the arena of strict science, is that repression has interceded to slow down or inhibit growth. How do I know? Some of my patients have reported foot growth, chest growth, breast growth and other kinds of growth after about a year of therapy. (We have a letter of a former patient who reported foot growth of several sizes after therapy). All that has happened in my therapy is lifting repression and liberating pain. If we reason backward we might say that repression prohibited proper growth from taking place. That means to me constant pressure in key sites against growth; against genetic destinations. And that again can mean the possibility of serious illness, possibly cancer. Pressure on the cells to stop this unfolding can be enormous. Until one has seen the liberation of pain it is difficult to comprehend.

So we can only say that one’s breasts are too small when we see if they grow as a result of this liberation. And I believe that will only happen when the patient arrives at deeply implanted pain, at birth and before, when so many hormones are affected; where so many set-points are dislocated and fixed. I think that, in this sense, the therapy may have an anti-cancer effect. Can you imagine the pressure our biology exerts to fulfill its genetic promise? That pressure continues against a constant pressure to hold it back. The result too often can be disease as the cells become deformed and dislocated. It is not only the obvious breasts and feet, which are, after all, measurable, but there my be so effects we cannot measure; for example, the kidneys, heart or liver. We see that wherever we have looked, (serotonin/impramine: natural killer cells) there are significant changes. We would expect the same with key organ systems. In other words, pain and repression are laid down as total experience, which means that just about every system is involved in the imprint of the memory. So we would expect that all key organ systems would be affected. That remains to be studied. But we would also expect that those systems, which are inherently weak and vulnerable, would be seriously affected by that repression. The answer? Have a good gestation and birth and infancy. Failing that, relive the key pains set down and undo the massive repression.

There are effects we cannot measure; for example, the kidneys, heart or liver. We see that wherever we have looked, (serotonin/impramine: natural killer cells) there are significant changes. We would expect the same with key organ systems. In other words, pain and repression are laid down as total experience, which means that just about every system is involved in the imprint of the memory. So we would expect that all key organ systems would be affected. That remains to be studied. But we would also expect that those systems, which are inherently weak and vulnerable, would be seriously affected by that repression. The answer? Have a good gestation and birth and infancy. Failing that, relive the key pains set down and undo the massive repression.

In writing about the imprint, I will note again that one way we know that very early imprinted pain endures is that many entering patients have high stress hormone levels which normalize after one year of the therapy. What this may mean is that the imprint endures, is a constant danger, and must be fought against. That danger is signaled by the high cortisol (stress hormone) levels. Why is it, then, that the levels come down to normal after a time? Because the imprint is no longer a force; It is now simply a memory. The force of the pain has been felt and integrated. It is not as though there is a reliving of the memory and then we find changes in the imprint; it is that the way the memory is held and engraved is through these various changes such as in stress hormone levels. The danger is no longer in evidence; the system can relax. The battle is over. As all systems normalize it means that there is no longer an irrevocable memory to deal with. The imprint as a total physiologic event no longer exists. Can we become neurotic again? Not in the same way because the harmful memory is gone. What we often cannot change are the secondary changes already in evidence due to the damage inflicted beforehand.

The Mystery Known as Depression, Part 6/12

6. THE NATURE OF THE IMPRINT

It seems that new research provides critical evidence on epigenetics, and how imprints through methylation can be passed down from one generation to another (Booij et al., 2013). A key could be repressed memory that endures and persists throughout our lives; it drives behavior, symptoms and aggravated depression. It turns out that imprints can be passed down from parents to baby and from grandparents to baby. Some genes which should be turned on are not, while those that should be off remain on. Critical in this process is methylation, which is a chemical reaction where a methyl group is transferred from a donor molecule (S-adenosylmethyonine) to the cytosine on DNA or a histone. The reaction is catalyzed by DNA methlytransferase (DNMT). A certain amount of methylation occurs naturally but trauma, such as maternal neglect in infancy, can cause excess methylation of key genes involved with the stress response. (Weaver et al, 2004) Methylation depends on the work of the chemical methyl group which is recruited when there is a traumatic event, and helps embed that memory. It seems that when there is a surge of methylation, part of it, the element 621-13, attaches or adheres to the gene. It is now part of the DNA and turns on or off certain hormones and other neuro-chemical processes. Once that happens and methyl is recruited, the genetic unfolding is thereafter altered.
In short, methylation can be an agent of (transcription) repression, or more exactly, a marker for it. In this context, repression is a systemic event that involves the whole body. If you reverse the methylation chemically (perhaps with new drugs they are developing), one can still have repression. But remove the repression through therapy and you may see demethylation. Until the studies are done, it's unclear how closely the two are linked, and in what tissues. A study at Duke University showed that when female mice were fed a diet rich in methyl it completed altered the fur pigment of the offspring. (Dolinoy, 2008) In other words, it acted like a genetic inheritance when it was not. It was the result of experience which is the linchpin of our theory--epigenetics.

In this context, traumatic events in very early childhood, (and I assume, including the period of gestation), leave a mark or tag on a gene that affects us possibly for life. They found that even grandparents affected the imprints of the grandchildren, which we will get to in a moment. But suffice to say that the experiences of our forebearers can endure and be passed down the genetic chain, the inheritance of acquired characteristics. This is something science thought impossible decades ago.

It is what we all know; that early love makes us stronger and less anxious. But it turns out that if the rat mothers were licked and groomed early on in their lives, that experience could be passed on to their offspring. The genes could be modified by the methyl group (and also other chemicals) in a beneficent way. In humans, that implies a good history in the mother means a good childhood for the children. And more loving by the mother, the less methylation in the child. And with less chronic stress hormone production there may be less chance of serious diseases later on, such as Alzheimer Disease.

To make sure that these changes in the rat pups resulted from experience and not hereditary, they let normally stable rat pups be raised by neurotic negligent mothers. And the result was still the same, unstressed babies. These babies had mothers who had normal amounts of methyl in their systems. Thus rats raised by loving mothers could pass it onto offspring even when the adopted mother was not loving. The genes for stress hormone output had minimal methylation. In other words love was passed down the genetic chain. So normal babies raised by negligent and inattentive mothers still had low methyl levels in their hippocampus. The babies started life one leg up, a good start in life despite a bad childhood. I believe that changes in the genes, methylation and acetylation, must occur very early as the whole neuronal system is evolving. So before we can state what causes depression or anxiety, we need to observe the early epigenetics at work. Again, pups born to unloving mothers were handed over to loving mothers, and those born to bad mothers reared by loving mothers still seemed to be normal and relatively unmethylated. Let us remember that methyl exists throughout the system but it is not the general amount of it but rather how much is found in specific genes (Weaver et al, 2004).

Another reason this research is important: they found that unloving mothers of rodents causes methylation of the estrogen receptors in female offspring. Then when they had offspring of their own the offspring were deficient in estrogen which made them less attentive and loving to their own babies. We as yet do not know how many key chemical processes can be affected by lack of early love. And more, we have no idea how many hormones are changed in neurotic mothers (heavily methylated) and how that affects myriad adult behaviors. Is depression inherited? There may be precursors for it which is never manifested if there were plenty of love later in childhood. Is some of the tendency to methylation inherited or epigenetically passed on? And does that form the basis for depression? It seems from the research just cited that that neurotic mothers (methylated), are ineluctably forced to be unloving, thus laying the groundwork for depression in the offspring later on (Weaver et al, 2004).

And what other hormones are depleted by this scenario? Are we born with a tendency to anxiety? Possibly, but then the imprint is not methyl so much as acetyl, in this case. With acetylation there are more faults in the repressive system. Acetylation (recruiting acetyl) pretty much produces the opposite of methylation, a tendency to open rather than close, toward expression rather than repression. The role of acetylation is inexact for now and requires further exploration.

Taken together these data suggest that trauma produced heavy methylation in those children who grew up in orphanages. And that process then affected much more in terms of brain and neuronal development. So when we find a mother who is not loving we need to know that she may being driven by her epigenes; she is a victim of those changes. Her cortisol/stress hormone level militates against maternal instincts. Methylation shuts down a number of “natural” behaviors. In neurosis we cannot be natural and appreciate nature because we are disconnected and alienated from our own nature, from our biography, history and feelings. We cannot rely on our feelings to guide us because they have effectively been shut down. Literally, the feelings are aliens. We have found in most patients but pronounced in depression, that patients on the verge of these feelings in sessions often run a fever. The body treats the feelings as a menace, a danger and something to be avoided; yet it is also what can liberate us.
Can we reverse or undo methylation? The research informs us that with rats who had been damaged, and raised by unloving mothers, when they were infused with trichostatin they did not show evident damage. As though the trauma never occurred. This drug removes methyl from the system. This is not exactly the same as demethylation. However, it did undo history (Weaver et al, 2004). This is what I think may be happening during the reliving and focusing on the imprint. There might be a change in methylation so as to reverse history; this is what we shall study in our future research projects. It seems to me the natural way provides far less possibility for collateral damage to the system. Since we already have found that chronically high cortisol levels have been reversed in our therapy, it would perhaps follow that methylation could also be reversed. In a way, the levels of methylation can be a marker for having been loved early on or not having been loved. We could tell more than the statements by the person who claims he was loved in his childhood if he were indeed not loved. How much denial is there?

Neurochemistry may be better relied on because biochemistry has no reason to lie and is not motivated by denial. It can be a marker for post traumatic stress. The more abuse as a child in these cases the more methylation produced. When we add this to our future research on telomeres and cortisol we will begin to have precise measures of the pain in us. And we will know when a drug is too dangerous for us, particularly the drugs like marijuana that tend to open us to ourselves; to our feelings and pain. Finally we will have a marker for the efficacy of certain psychotherapies. Does the therapy undo the past? Does it help relieve repression and therefore depression? Is there great first line pain in anxiety states? What seems to be the case is that love obviates methylation and produces normal beings.

K. J. S. Anand and associates state that in a number of suicides by violent means “the significant risk factors were those perinatal events that were likely to cause pain in the newborn.” (Anand & Scalzo, 2000) (More on the link between suicide and perinatal trauma below.) They also point out the carrying mothers who smoke heavily had babies more prone to criminality later on. And mothers who took drugs while pregnant had children far more prone to drug use, both serious opiates (morphine) and speed (amphetamine).

There are literally hundreds of studies now to bolster the hypothesis about early imprints, how they last and alter our systems. Some twenty years ago, most of this research had not been thought of. (Again, this is discussed in detail in Primal Healing. (Janov, 2006) In another revealing study carried out in Canada in 1998, David P. Laplante and Michael L. Meaney of Montreal’s McGill University looked at women who were pregnant during a severe ice-storm to assess the long-term effects of stress on their offspring. (Laplante, et al., 2004) The researchers write: “We suspect that high levels of prenatal stress exposure particularly in early in pregnancy, may negatively affect the brain development of the fetus... Imprinting at birth may predispose individuals to certain patterns of behavior that remain masked throughout most of adult life.”